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NDT Advance Access originally published online on November 25, 2005
Nephrology Dialysis Transplantation 2006 21(2):281-284; doi:10.1093/ndt/gfi291
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Editorial Review

Progression versus regression of chronic kidney disease

Agnes B. Fogo

Department of Pathology, Vanderbilt University Medical Center, Nashville, TN 37232, USA

Correspondence and offprint requests to: Agnes B. Fogo, MD, MCN C3310, Department of Pathology, Vanderbilt University Medical Center, Nashville, TN 37232, USA. Email: agnes.fogo@vanderbilt.edu

Keywords: ACEI, angiotensin; ARB; capillary branching; PAI-1; podocyte

The first 150 words of the full text of this article appear below.



   Introduction
 
Chronic kidney disease (CKD) is a major cause of morbidity and mortality worldwide, and is characterized by relentless progressive scarring of renal parenchyma that ultimately results in end-stage renal disease with the need for dialysis or transplantation. Scarring is, however, not an inherently irreversible process, as it may be modulated in, for example, skin, heart and large arteries. However, the kidney has unique challenges in remodelling of glomerulosclerosis, in that nephron development ends in late gestation, and generation of new glomeruli is not possible after term birth. The apparent inexorable progression characteristic of CKD is postulated to start with disease-specific initial scarring that then activates compensatory but ultimately maladaptive changes in the remaining nephrons. These compensatory changes include haemodynamic alterations and altered growth responses that promote further scarring and fuel this vicious circle [1]. It is of interest that this sclerotic process is not static, in that even . . . [Full Text of this Article]



   Feasibility of regression—proof of principle in experimental models
 


   Mechanisms of regression
 
Multipronged interventions
Effects on extracellular matrix (ECM)
Cell responses


   Limits for induction of regression
 


   Summary
 

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